Horm Metab Res 1990; 22(12): 608-611
DOI: 10.1055/s-2007-1004984
Originals Basic

© Georg Thieme Verlag, Stuttgart · New York

ACTH1-24 Stimulates Muscle Cell Glucose Uptake

P. A. Levin, T. Bistritzer, L. Hanukoglu, S. R. Max, L. M. Roeder
  • Departments of Pediatrics (PAL, TB, LH, LMR), Medicine (PAL) and Neurology (SRM), University of Maryland School of Medicine, Baltimore, Maryland, and the Medical Biotechnology Center of the Maryland Biotechnology Institute, University of Maryland (SRM), Baltimore, Maryland, U. S. A.
Further Information

Publication History



Publication Date:
24 April 2008 (online)


3H-2-deoxyglucose (2-DG) uptake was measured in L6A-1 rat skeletal muscle cells (a rapidly fusing subclone of L6), following addition of several concentrations (10-16 to 10-9M) of the N-terminal fragment of ACTH1-24 to cells deprived of serum and insulin for 21 hours, but maintained in the presence of (5 μg/ml) insulin (stimulated state). There was a marked dose-dependent increase of 2-DG uptake at the various ACTH1-24 (P < 0.001). There was no correlation between the time of exposure of the cells to serum-free conditions and the rate of uptake of 2-DG at the various ACTH1-24 Concentrations both in the basal and insulin-stimulated states. Addition of catochalasin B (50 μM) to the cells, which inhibited both basal and insulin-stimulated uptake of 2-DG (by 70% and 91%, respectively) completely eliminated the enhancement of both of these uptake rates to 10-12 MACTH 1-24 The results suggest that: 1) ACTH1-24 stimulates carrier-mediated uptake of glucose in skeletal muscle cells. 2) The site of action of ACTH1-24 is on the non-insulin mediated glucose uptake (NIMGU) system. 3) ACTH1-24 may be a useful probe to delineate some of the events associated with the NIMGU pathway.